PuSH - Publication Server of Helmholtz Zentrum München: MAPK phosphatase-1 represents a novel anti-inflammatory target of glucocorticoids in the human endothelium.

Information

Clues to quality of journals

Open Access Policy of Helmholtz Association 2016

CC Licencences

Publication Metrics

Navigation

Home

Deutsch

EVA: Electronic Publishing

New EVA Application

Research

Advanced Search

Browse by ...

... HMGU-Authors/Consortia

... Organizational Structure

... Journal

... Publication Type

... Research Data

... Arbeitsgruppen

... Publication Year

Publication overview

Statistics

Statistics (last 5 years)

OA Publications

Publish

Submit Publication

Import publication from...

...EVA

Report missing publication

Highlights

Support & Contact

Contact persons

Help

Data protection

Helmholtz Open Science

JANE Journal Estimator

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Fürst, R.* ; Schroeder, T. ; Eilken, H.M. ; Bubik, M.F.* ; Kiemer, A.K.* ; Zahler, S.* ; Vollmar, A.M.*

MAPK phosphatase-1 represents a novel anti-inflammatory target of glucocorticoids in the human endothelium.

FASEB J. 21, 74-80 (2007)

Publ. Version/Full Text Volltext

DOI

PMC

	Closed

Abstract
Metrics
Extra information

Glucocorticoids are well-established anti-inflammatory drugs thought to mainly act by inhibition of proinflammatory transcription factors like NF-{kappa}B. In recent years, however, transcription factor-independent mechanisms of glucocorticoid action have been proposed, namely the influence on MAPK pathways. Here we identify MAPK phosphatase-1 (MKP-1) as a pivotal mediator of the anti-inflammatory action of glucocorticoids in the human endothelium. We applied dexamethasone (Dex) to TNF-{alpha}-activated human endothelial cells and used the adhesion molecule E-selectin as inflammatory read-out parameter. Dex is known to reduce the expression of E-selectin, which is largely regulated by NF-{kappa}B. Here, we communicate that Dex at low concentrations (1–100 nM) markedly attenuates E-selectin expression without affecting NF-{kappa}B. Importantly, Dex is able to increase the expression of MKP-1, which causes an inactivation of TNF-{alpha}-induced p38 MAPK and mediates inhibition of E-selectin expression. In endothelial MKP-1–/– cells differentiated from MKP-1–/– embryonic stem cells and in MKP-1-silenced human endothelial cells, Dex did not inhibit TNF-{alpha}-evoked E-selectin expression. Thus, our findings introduce MKP-1 as a novel and crucial mediator of the anti-inflammatory action of glucocorticoids at low concentrations in the human endothelium and highlight MKP-1 as an important and promising anti-inflammatory drug target.—Fürst, R., Schroeder, T., Eilken, H. M., Bubik, M. F., Kiemer, A. K., Stefan Zahler, S., Vollmar, A. M. MAPK phosphatase-1 represents a novel anti-inflammatory target of glucocorticoids in the human endothelium

Impact Factor

Scopus SNIP

Web of Science
Times Cited

Scopus
Cited By

Altmetric

6.721

1.383